Abstract
Hypocalcemia and hyperphosphatemia are the pathognomonic biochemical features of hypoparathyroidism, and result directly from lack of parathyroid hormone (PTH) action on the kidney. In the absence of PTH action, the renal mechanisms transporting calcium and phosphate reabsorption deregulate, resulting in hypocalcemia and hyperphosphatemia. Circulating calcium negatively regulates PTH secretion. Hypocalcemia causes neuromuscular disturbances ranging from epilepsy and tetany to mild paresthesia. Circulating phosphate concentration does not directly regulate PTH secretion. Hyperphosphatemia is subclinical, but chronically promotes ectopic mineralization disease. Vitamin D-thiazide treatment leads to ectopic mineralization and renal damage. PTH treatment has the potential for fewer side effects.
